segunda-feira, 11 de junho de 2012

Staphylococcus hominis

Staphylococcus hominis is a coagulase-negative member of the bacterial genus Staphylococcus, consisting of Gram-positive, spherical cells in clusters. It occurs very commonly as a harmless commensal on human and animal skin. However, like many other coagulase-negative staphylococci, S. hominis may occasionally cause infection in patients whose immune systems are compromised, for example by chemotherapy or predisposing illness.

DescriptionColonies of S. hominis are small, usually 1–2 mm in diameter after 24 hours' incubation at 35 °C, and white or tan in colour. Occasional strains are resistant to novobiocin and may be confused with other resistant species (e.g. S. saprophyticus.)

It is one of only two species of Staphylococcus that display sensitivity to desferrioxamine, the other being S. epidermidis. Unlike S. epidermidis, S. hominis produces acid from trehalose, so the two tests together serve to identify the species.

[edit] BiologyNumerous coagulase-negative staphylococci appear commonly on the skin of human. Of these species, Staphylococcus epidermidis and S. hominis are the most abundant. While S. epidermidis tends to colonize the upper part of the body, S. hominis tends to colonize in areas with numerous apocrine glands, such as axillae and the pubic region. In a certain study, S. hominis was calculated to account for 22% of the total staphylococci species recovered from individuals, second to S. epidermidis at 46%. S. hominis is the predominant species on the head, axillae, arms, and legs. S. hominis, as well as most other staphylococci species common on the human skin, is able to produce acid aerobically from glucose, fructose, sucrose, trehalose, and glycerol. Some strains were also able to produce acid from turanose, lactose, and galactose, melezitose, mannitol, and mannose. Most strains colonize on the skin for relatively short periods of time compared to other Staphylococcus species. They, on average, stay on the skin for only several weeks or months. The cell wall contains low amounts of teichoic acid and glutamic acid. The cell wall teichoic acid contains glycerol and glucosamine. S. hominis cells are Gram-positive cocci, usually 1.2 to 1.4 micrometers in diameter. They appear normally in tetrads and sometimes in pairs.[1]

[edit] ResistanceBased on a total of 240 strains, all were resistant to lysozyme, some were slightly resistant to lysostaphin, 77% were susceptible to penicillin G, 97% to streptomycin, 93% to erythromycin, 64% to tetracycline, and 99% to novobiocin.[2]

[edit] CulturingWhen grown in agar cultures, colonies are usually circular, 4.0 to 4.5 micrometers in diameter. Agar colonies usually have wide edges and an elevated center. They are commonly smooth with dull surfaces, and are yellow-orange pigmented in the center of the opaque colonies. They grow both in aerobic and anaerobic conditions, but tend to grow significantly less in the latter. Optimal NaCl concentrations of the agar culture for the growth of S. hominis seems to be around 7.5%, and a salt concentration of 15% yielded poor growth to no growth at all. The optimal growth temperature range was around 28 to 40 °C, but good growth is still observed at 45 °C, while no growth is observed at 15 °C. S. hominis can be differentiated from staphylococci by its colony morphology and pigmentation patterns, predominant tetrad cell arrangement, poor growth in thioglycolate, low tolerance of NaCl, and carbohydrate reaction pattern. Each species is also significantly different in cell wall composition, lactic acid configuration, temperature extremes of growth, coagulase activity, hemolysis acetylmethylcarbinol production, nitrate reduction, and phosphatase, DNase, and bacteriolytic activities. Similarities in these properties between S. hominis and several other species suggest there is a close relationship between S. hominis and S. epidermidis, S. haemolyticus, and S. warneri.[3]

[edit] Antibiotic-resistant subspeciesS. hominis is normally found on human skin and is usually harmless, but can sometimes cause infections in people with abnormally weak immune systems. Most, if not all, strains are susceptible to penicillin, erythromycin, and novobiocin, but a divergent strain, S. hominis subsp. novobiosepticus (SHN) was found recently. This strain was named so because of its unique resistance to novobiocin and its failure to produce acid aerobically from trehalose and glucosamine. In addition, the 26 isolated strains of this new subspecies are resistant to nalidixic acid, penicillin G, oxacillin, kanamycin and streptomycin. They were also somewhat resistant to methicillin and gentamicin, and most strains were resistant to erythromycin, clindamycin, chloramphenicol, trimethoprim/sulfamethoxazole and ciprofloxacin, as well. In addition, S. hominis subsp. hominis is commonly found isolated from human skin, but there are no reports of the isolation of SHN from the human skin.[4]

The SHN is so similar to the original S. hominis, now called S. hominis subsp. hominis, that a MicroScan system that clinical microbiology laboratories use identified seven of 31 S. hominis subsp. novobiosepticus cultures as S. hominis subsp. hominis. The relationship between the two is currently unknown, but antibiotic-resistant isolates of S. hominis belong only to SHN. [5]

SHN strains seems to have thickened cell walls, and this tendency may be the result of a genetic background that also allows for vancomycin resistance. The thickened cell walls exist in subspecies with and without vancomycin resistance which suggests this subspecies did not originate from the acquiring of resistance genes. [6]

[edit] OriginThe combined resistance to novobiocin and oxacillin is hypothesized to have originated from a simultaneous introduction of genes controlling the resistance to the two. These genes were believed to have been acquired originally through heterologous DNA from a methicillin-resistant strain of one of the novobiocin-resistant species belonging to the S. sciuri or the S. saprophyticus groups. The larger genome size of the SHN compared to that of S. hominis subsp. hominis may be the result of the acquiring of heterologous DNA. This new, divergent strain was first described in 1998, and this microbe was first implicated in causing bactermia in 2002. Another hypothesis is the insertion of the mec A gene and its flanking sequence into the chromosome of SHN might have affected the expression of a closely linked gene, which converted the host to become novobiocin-resistant.[7]